Technical Abstract:
Fumonisins are polyketide mycotoxins that are produced in maize kernels by the fungus Gibberella fujikuroi mating population A (MP-A) (anamorph, Fusarium moniliforme, syn. F. verticillioides). These toxins are carcinogens in rats and mice and there is an epidemiological correlation between the consumption of fumonisin contaminated maize and human esophageal cancer in some areas of the world. Researchers are employing biochemical, genetic, and molecular genetic approaches to study fumonisin biosynthesis. We used PCR with a cDNA template and degenerate primers to isolate a gene (FUM5) that has sequence homology to bacterial and fungal Type I PKS genes. Inactivation of FUM5 via gene disruption reduced fumonisin production by over 99% in G. fujikuroi MP-A. These data are consistent with FUM5 encoding a PKS that catalyzes the synthesis of the linear carbon backbone of fumonisins. Because classical genetic studies indicate that fumonisin biosynthetic genes may be clustered, we have begun sequencing the DNA flanking FUM5 in search of other genes. To date, we have identified four open reading frames (ORFs). Comparisons of the predicted translation products of these ORFs with protein sequence databases suggest that the ORFs may function in fumonisin biosynthesis. We are beginning to understand the process of fumonisin biosynthesis as a result of the studies described above and others. We anticipate that a clear understanding of this process will reveal weak links that can be exploited to control fumonisin contamination in maize.